Involvement of cell calcium and transmembrane potential in control of hepatocyte volume
Involvement of cell calcium and transmembrane potential in control of hepatocyte volume
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细胞钙和跨膜电位参与肝细胞体积的控制
DOI：
10.1002/hep.1840130527
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发表时间：
1991
期刊：
影响因子：
13.5
通讯作者：
R. Wondergem
中科院分区：
文献类型：
--
作者：
W. Khalbuss;R. Wondergem
本研究探讨了肝细胞钙和细胞骨架在低渗应激诱导的肝细胞跨膜电位增加和细胞体积控制的激活中的作用。在暴露于低渗介质之前和之后，通过玻璃微电极测量小鼠肝脏切片中的肝细胞跨膜电位。通过将肝切片短暂暴露于制霉菌素（一种阳离子成孔抗生素），使肝细胞装载四甲基铵。肝细胞稳态水量的变化是通过暴露于低渗介质 4 分钟后用四甲基铵敏感的双管微电极测量的细胞内四甲基铵活性的变化来确定的。对照渗透压 (∼280 mOsm) 74% 的低渗应激使肝细胞跨膜电位超极化为对照肝细胞跨膜电位的 1.83 倍，细胞水量增加 1.19 倍。 Ca2+通道阻滞剂维拉帕米（100 μmol/L）完全抑制低渗应激引起的肝细胞跨膜电位超极化。这种抑制作用在 37.5 或 50 μmol/L 剂量时减弱，但与对照相比，这些超极化也显着降低。与对照组相比，添加维拉帕米剂量（50 μmol/L）期间的低渗应激也导致细胞肿胀增加 23%。无 Ca2+ 培养基加上乙二醇-双（β-氨基乙基醚）-N,N'-四乙酸（5 mmol/L）可抑制低渗应激引起的肝细胞跨膜电位增加，并导致与对照相比细胞肿胀增加 16%。钙调蛋白抑制剂三氟拉嗪 (100 μmol/L) 和异丙嗪 (100 μmol/L) 抑制低渗透压引起的肝细胞跨膜电位超极化，3,4,5-三甲氧基苯甲酸酯 8-(N,N-二乙氨基)辛酯) (50 μmol/L) 也能抑制细胞内储存的 Ca2+ 的动员。细胞松弛素 B (50 μmol/L) 可破坏微丝，还可抑制渗透应激引起的肝细胞跨膜电位超极化。相比之下，相同条件下的秋水仙碱（10 μmol/L）则没有效果。这些结果表明，细胞外和细胞内钙、钙调蛋白系统和微丝参与控制和激活低渗应激诱导的肝细胞肝细胞跨膜电位增加。肝细胞跨膜电位的这些变化在细胞体积调节中发挥作用。 （肝病学 1991；13：962–969。）
This study examined the role of hepatocyte calcium and cytoskeleton in activation of hyposmotic stress‐induced increases in hepatocyte transmembrane potential and control of cell volume. Hepatocyte transmembrane potential was measured by glass microelectrodes in mouse liver slices before and after exposure to hyposmotic medium. Hepatocytes were loaded with tetramethylammonium by briefly exposing liver slices to nystatin, a cation poreforming antibiotic. Changes in hepatocyte steady‐state water volume were determined by changes in intracellular tetramethylammonium activity measured with tetramethylammonium‐sensitive, double‐barrel microelectrodes 4 min after exposure to hyposmotic medium. Hyposmotic stress of 74% of the control osmolality (∼280 mOsm) hyperpolarized hepatocyte transmembrane potential by 1.83 times the control hepatocyte transmembrane potential, and cell water volume increased by a factor of 1.19. The Ca2+ channel blocker verapamil (100 μmol/L) completely inhibited hyposmotic stress‐induced hyperpolarization of hepatocyte transmembrane potential. This inhibitory effect diminished at doses of 37.5 or 50 μmol/L, but even these hyperpolarizations were decreased significantly compared with control. Hyposmotic stress during added verapamil dosage (50 μmol/L) also resulted in 23% greater cell swelling compared with control. Ca2+ free medium plus ethylene glycol‐bis (β‐aminoethylether)‐N,N'‐tetraacetic acid (5 mmol/L) inhibited hyposmotic stress‐induced increases in hepatocyte transmembrane potential and resulted in 16% greater cell swelling compared with control. Calmodulin inhibitors trifluoperazine (100 μmol/L) and promethazine (100 μmol/L) inhibited the hyperpolarization of hepatocyte transmembrane potential caused by hyposmolality, as did 3,4,5‐trimethoxybenzoate 8‐(N,N‐diethylamino)octyl ester) (50 μmol/L), which inhibits mobilization of Ca2+ from intracellular stores. Cytochalasin B (50 μmol/L), which disrupts microfilaments, also inhibited hyperpolarization of hepatocyte transmembrane potential with osmotic stress. In contrast, colchicine (10 μmol/L) under identical conditions had no effect. These results show that extracellular and intracellular calcium, the calmodulin system and microfilaments are involved in control and activation of hyposmotic stress‐induced increases in hepatocyte hepatocyte transmembrane potential. These changes in hepatocyte transmembrane potential play a role in cell volume regulation. (HEPATOLOGY 1991;13:962–969.)
静止和白细胞介素 2 刺激的 T 淋巴细胞对低渗的体积反应。
DOI：
10.1152/ajpcell.1988.254.2.c286
发表时间：
1988
期刊：
The American journal of physiology
影响因子：
--
作者：
Lee,SC;Price,M;Prystowsky,MB;Deutsch,C
通讯作者：
Deutsch,C
钙拮抗剂 TMB-8 对兔回肠活性 Na 和 Cl 转运的影响。
DOI：
10.1152/ajpgi.1986.250.5.g691
发表时间：
1986
期刊：
The American journal of physiology
影响因子：
--
作者：
Donowitz,M;Cusolito,S;Sharp,GW
通讯作者：
Sharp,GW